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Archives Of Research News Blog From Medicineworld.Org

February 15, 2006, 11:27 PM CT

Discovery That May Lead to New Treatments

Discovery That May Lead to New Treatments The image above at left shows normal blood vessels in a mouse paw. Five minutes after receiving arthritis-causing antibodies, the blood vessels become leaky, as shown at right. Photo by Bryce Binstadt, M.D., Ph.D., and Pratik Patel Courtesy Joslin Diabetes Center and Massachusetts General Hospital
What makes joints in people with rheumatoid arthritis, and related conditions like Lyme disease or lupus, so susceptible to attack by the body's immune system, leading to painful flare-ups and deterioration? The answer may surprise you.

The answer did surprise researchers at Joslin Diabetes Center and Massachusetts General Hospital (MGH) in Boston, who gained a novel insight into this question in a recent collaborative study. Their report appeared in the January 29 online issue of Nature Immunology, and is scheduled to appear in the February print edition.

Working with an animal model of rheumatoid arthritis, the scientists discovered that histamine, a small molecule commonly associated with asthma and allergy, is produced as part of the inflammatory process during the development of arthritis. Histamine made the blood vessels surrounding the joints particularly vulnerable to leakage, and thereby rendered the joints more susceptible to inflammatory attack. The scientists think that this is true not only in rheumatoid arthritis, but perhaps also in other autoimmune conditions with which arthritis is associated, such as lupus, and in some infectious diseases, like Lyme disease.

"For patients with rheumatoid arthritis, these new findings raise the possibility that medications designed to prevent the blood vessels from becoming leaky might one day be used to delay the onset of arthritis or to prevent flare-ups of disease," said Christophe Benoist, M.D., Ph.D., who led the study together with Diane Mathis, Ph.D., and Ralph Weissleder, M.D., Ph.D. Drs. Mathis and Benoist head Joslin's Section on Immunology and Immunogenetics, hold the William T. Young Chair in Diabetes Research at Joslin, and are Professors of Medicine at Harvard Medical School. Dr. Weissleder heads the Center for Molecular Imaging Research at MGH and is a Professor of Radiology at Harvard Medical School.........

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February 10, 2006, 7:39 PM CT

Explaining Alzheimer's Memory Loss

Explaining Alzheimer's Memory Loss
Based on laboratory research, researchers at Georgetown University Medical Center have a new theory as to why people with Alzheimer's disease have trouble performing even the simplest memory tasks, such as remembering a family member's name.

That's because they discovered a physical link between apolipoprotein E (APOE), the transport molecules known to play a role in development of the disease, and glutamate, a brain chemical necessary for establishing human memory.

As per a research findings reported in the Journal of Biological Chemistry, the research team specifically found that receptors on the outside of brain nerve cells (neurons) that bind on to APOE and glutamate are connected on the surface of neurons, separated from each other by only a small protein.

While the scientists don't know why these receptors are linked together, they say inefficient or higher-than-average levels of APOE in the brain could possibly be clogging these binding sites, preventing glutamate from activating the processes necessary to form memories.

"We have found out that two receptors previously thought to have nothing to do with each other do, in fact, interact, leading us to conclude that APOE affects the NMDA glutamate channel that is important in memory," says the study's senior author, G. William Rebeck, PhD, associate professor of neuroscience in Georgetown's Biomedical Graduate Research Organization.........

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February 8, 2006, 10:55 PM CT

Broccoli And Cauliflower For Cancer Protection

Broccoli And Cauliflower For Cancer Protection
Naturally occurring chemicals found in certain vegetables, like broccoli, cauliflower and cabbage, can enhance DNA repair in cells, perhaps helping to stop them becoming malignant, as per a report reported in the British Journal of Cancer* today (Tuesday).

The researchers, based at Georgetown University in Washington DC, have shown that a compound called I3C** found in these vegetables, and a chemical called genistein found in soy beans, both increase the levels of vital DNA repair proteins in cancer cells. Eventhough population studies have suggested a link between eating such vegetables and protection against cancer before, this study now puts forward a molecular mechanism on how they might work.

The repair proteins, regulated by genes called BRCA1 and BRCA2, are important for preventing damaged genetic information being passed on to the next generation of cells. If people have a faulty BRCA gene they are at a higher risk of developing some forms of cancer, including breast, ovarian and prostate cancer. Since decreased amounts of the BRCA proteins are seen in cancer cells, higher levels might prevent cancer developing. The ability of I3C and genistein to boost the amount of BRCA proteins could explain their protective effects.

Professor Eliot M. Rosen, senior author of the report, said: "Studies that monitor people┬┐s diets and their health have found links between certain types of food and cancer risk. However, before we can say a food protects against cancer, we have to understand how it does this at a molecular level".........

Posted by: Janet      Permalink

February 8, 2006, 10:46 PM CT

DNA repair mystery solved

DNA repair mystery solved
Cancer Research UK researchers believe the final piece of the picture of how cells fix a severe type of DNA damage - thereby reducing the chances that the cells become malignant - will fall into place tomorrow (Friday) when they publish their latest findings in the journal Cell*.

Professor Steve Jackson, based at Cambridge University, discovered the first component of one particular DNA repair process over ten years ago. More pieces were found, and eventually researchers thought they had the whole process mapped out. But recent evidence came to light that suggested there was still one bit missing. Now Prof Jackson has finished what he started by discovering a new molecule that completes the picture.

The molecule is called XLF** and while it may have a role in causing cancer, it can possibly also be targeted by new cancer therapys - for example, blocking the action of XLF in cancer cells could 'soften up' the cells and allow radiotherapy to deliver more easily a knockout blow.

Prof Jackson said: "You could say we went fishing. We know molecules in these processes tend to bind together in order to work, so Peter Ahnesorg - a PhD student in my laboratory - used an established component of the repair pathway as bait and cast it into a sea of proteins. Then he pulled out the bait and examined what was stuck to it.........

Posted by: Scott      Permalink

February 8, 2006, 10:28 PM CT

Aging Cells In An Aging Body

Aging Cells In An Aging Body
Brown University biologists have uncovered intriguing evidence to support the theory that old cells help make old bodies. In a study of baboons, researchers showed that as these animals age, the number of aging cells in their skin significantly increases.

Over time, cells lose their ability to divide, a state known as replicative senescence. The new research, published in an advanced online edition of Science, is the first to quantify the presence of replicatively senescent cells in any species.

"For 40 years, we've known about replicative senescence," said John Sedivy, a Brown professor of medical science and the senior scientist on the project. "Whether it promotes the aging of our bodies, however, is highly controversial. While it may make intuitive sense, skeptics say 'Show us the evidence.' The first solid evidence is in this study. These initial findings won't settle the debate, but they make a strong case".

Human cells replicate anywhere from 60 to 90 times before senescence sets in, a phenomenon researchers believe is a safeguard against disease. While senescent cells still function, they don't behave the way young cells do - and are associated with skin wrinkles, delayed wound healing, weakened immune system response and age-related diseases such as cancer.........

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January 26, 2006, 4:23 PM CT

Hunting For Cancer Cure

The New Cancer Hunters Image courtesy of IsraCast
Scientists from the Hebrew University have succeeded in isolating a variant of the Newcastle Disease Virus (NDV-HUJ), which commonly affects birds, in order to specifically target cancer cells. The research, which has already cleared the first phase of clinical trials, is already patented and if all goes well it might receive an approval for clinical use, changing the way we think about viruses forever.

Professors Amos Panet and Zichria Zakay-Rones, from the Department of Virology at the Hebrew University Hadassah Medical School, have been involved during the past five years in research that could create a new and effective weapon in the fight against cancer, as well as change the way we look at viruses. As an obligatory parasitic entity with no independent life of its own, a virus must enter a living cell in order to multiply. The viral life-cycle begins when the virus inserts its genetic material into the host's cell, forcing it to replicate the virus' components, and eventually leading to the death of the cell. The NDV-HUJ virus, discovered by the Hebrew University in Jerusalem team, acts in a similar way, except for its outstanding preference for infecting malignant cells. NDV-HUJ is a natural variant of NDV (Newcastle Disease Virus) which commonly affects birds. Being an attenuated variant (e.g., weakened virus), it is innately preferentially targets and replicates in certain types of tumor cells, leaving normal cells almost unaffected.........

Posted by: Janet      Permalink

January 26, 2006, 11:52 AM CT

Link Between Cat Faeces And Schizophrenia

Link Between Cat Faeces And Schizophrenia
Research published recently in Procedings of the Royal Society B, shows how the invasion or replication of the parasite Toxoplasma gondii in rats may be inhibited by using anti-psychotic or mood stabilising drugs.

The scientists tested anti-psychotic and mood stabilising medications used for the therapy of schizophrenia on rats infected with T. gondii and found they were as, or more, effective at preventing behaviourial alterations as anti-T. gondii drugs. This led them to think that T. gondii may have a role in the development of some cases of schizophrenia.

Dr Joanne Webster from Imperial College London, and lead researcher said: "Eventhough we are certainly not saying that exposure to this parasite does definitely lead to the development of schizophrenia, this and prior studies do show there may be a link in a few individuals, providing new clues for how we treat toxoplasmosis and schizophrenia".

Prior epidemiological and neuropathological studies have indicated some cases of schizophrenia may be associated with environmental factors, such as exposure to the parasite T. gondii. At the same time several of the medications used to treat schizophrenia have been shown to posess anti-parasitic and in particular anti-T.gondii properties. This led the authors to suspect that the anti-psychotic activity of these medications may be due to their inhibition of these parasites.........

Posted by: Daniel      Permalink

January 25, 2006, 9:01 PM CT

Defective Synapse Generator Leads To Alzheimer

Defective Synapse Generator Leads To Alzheimer
A new UCLA/Veterans Affairs study implicates defects in the machinery that creates connections between brain cells as responsible for the onset of Alzheimer disease.

The defect in PAK enzyme signaling pathways - vital to creation of these connections, or synapses - is correlation to loss of a synapse protein in certain forms of mental retardation, such as Down syndrome. The new finding suggests therapies designed to address the PAK defect could treat cognitive problems in both patient populations.

The peer-reviewed journal Nature Neuroscience published the study online Jan. 15.

"The emerging lesson is that cognitive problems in Alzheimer disease are correlation to defects in the machinery controlling neuronal connections, not the lesions observed by pathologists," said principal investigator Greg Cole, professor of medicine and neurology at the David Geffen School of Medicine and Alzheimer Disease Research Center at UCLA, and the Geriatric Research Education and Clinical Center at the Veterans Affairs Greater Los Angeles Health Care System and Sepulveda Ambulatory Care Center. "Our findings show that PAK defects in the brains of Alzheimer patients appear sufficient to directly cause cognitive difficulties".

In some families, early-onset Alzheimer disease can be caused by mutations in different genes that all increase the production of a sticky protein called Abeta42 (Ab42). The increase causes the protein to form aggregates, little clusters or long filaments that pile up and make lesions in the brain called plaques.........

Posted by: Daniel      Permalink

January 25, 2006, 8:51 PM CT

Nano Motor Powered By Solar Energy

Nano Motor Powered By Solar Energy Image courtesy of UCLA
Chemists at Italy's University of Bologna, UCLA and the California NanoSystems Institute have designed and constructed a molecular motor of nanometer size that does not consume fuels; their nano motor is powered only by sunlight. The research, federally funded by the National Science Foundation, will be published Jan. 31 in Proceedings of the National Academy of Sciences (PNAS).

The nano motor can work continuously without any external interference, and operates without consuming or generating chemical fuels or waste, said Fraser Stoddart, UCLA's Fred Kavli Professor of NanoSystems Sciences and director of the institute.

"We design and make sunlight-powered nano motors and then 'test drive' them much as an engineer would a new motorcar," Stoddart said. "It is as if we had managed to get a solar-powered motor car onto the road and running".

Precisely how light-powered nano motors will be used in the future is still not clear, Stoddart said, but he listed many possible areas for applications: nanoelectronics, molecular computers and nano valves that perhaps could be used for the delivery of anti-cancer drugs and other medications.

"The achievement reported in PNAS is the culmination of a research effort lasting a quarter of a century and involving hundreds of students and millions of dollars," Stoddart said.........

Posted by: Scott      Permalink

January 24, 2006, 9:38 PM CT

Resistance Patterns To Aids Drugs

Resistance Patterns To Aids Drugs
Some HIV medications lead to the development of drug-resistant HIV when patients take as few as two percent of their medications. For other medications, resistance occurs only when patients take most of their pills. These differences appear to be explained by the different levels of viral "fitness" of the drug-resistant HIV, say AIDS scientists in a new study.

The research, led by David Bangsberg, MD, MPH, an AIDS specialist at the University of California, San Francisco, is published in the January 9 issue of the journal AIDS.

Viral "fitness" refers to the inherent ability of a virus to replicate and cause disease. Incomplete pill-taking by patients causes HIV to mutate and become resistant to the effects of the medications, while the medications that were consumed, in turn, cause the newly resistant virus to become less fit.

The type of medicine also factors in. Differences in viral fitness of mutated resistant virus occur between different classes of antiretroviral drugs, said Bangsberg, who is an associate professor of medicine at UCSF and director of the UCSF Epidemiology and Prevention Interventions Center at San Francisco General Hospital Medical Center.

When patients succeed in completely suppressing HIV, which requires that patients take all or almost all of their medications as directed, resistant strains either do not occur or are suppressed, he added.........

Posted by: Mark      Permalink

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Did you know?
Scientists at Yale have brought to light a mechanism that regulates the way an internal organelle, the Golgi apparatus, duplicates as cells prepare to divide, according to a report in Science Express.Graham Warren, professor of cell biology, and colleagues at Yale study Trypanosoma brucei, the parasite that causes Sleeping Sickness. Like a number of parasites, it is exceptionally streamlined and has only one of each internal organelle, making it ideal for studying processes of more complex organisms that have a number of copies in each cell. Archives of research news blog

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